Human periodontitis is a chronic inflammatory disease of the periodontium characterized by bursts of disease activity and longer periods of remission. Ligature-induced periodontitis provides a model with a similar microflora in which the rate of disease can be accelerated. Previous studies have demonstrated that immunization with heat killed Bacteroides macacae provides some protection in the ligature induced periodontitis model by reducing both the recolonization by B. macacae and the extent of alveolar bone loss compared to the sham-immunized, ligated and immunized, mon-ligated controls. This proposal extends these earlier observations and attempts to enhance the "protective" humoral response and evaluate which bacterial factors are responsible for modifying the pathogenesis of ligature induced periodontitis. The specific aims are to: 1. Isolate capsular and membrane fractions from B. macacae. 2. Identify the fraction(s) most likely to evoke a protective response. Monkey sera available from the previous grant supported studies and rabbit antisera to the fractions will be prepared ad evaluated by in vitro assays for their potential influence on colonization and infectivity. These will include the effects of antisera to the fractions on opsonization, coaggregation with other oral bacteria, and adherence to epithelial cells. 3. Examine the effects of immunization with the selected bacterial fraction on ligature-induced periodontitis in monkeys. This will be characterized on the basis of clinical, histological, microbiological and immunological. 4. Evaluate how immunization confers protection during ligation. Factors to be considered include tissue invasion by the bacteria, serum opsonization of the bacteria, bacterial co-aggregation, and bacterial adherence to epithelium. This proposal would provide a better understanding of the pathogenesis of periodontitis and would potentially be of value in treatment.